Objective To investigate the effects of remifentanil postconditioning and combined remifentanil-prupofol postconditioning on liver ischemia-reperfusion (I/R) injury in rats.Methods Thirty male SD rats weighing 220-280 g were randomly divided into 5 groups ( n =6 each):group sham operation (group Ⅰ ) ; group I/R (group Ⅱ ) ; group propofol postconditioning (group Ⅲ ) ; group remifentanil postconditioning (group Ⅳ ) and group combined propofol-remifentanil postconditioning (group Ⅴ ).In groups Ⅱ- Ⅴ the hepatic arteries and veins of middle and left were occluded for 30 min.In groups Ⅲ-Ⅴ propofol ( at 30 mg· kg- 1 · h - 1 ) and/or remifentanil (at 1 μg· kg- 1 · min- 1 ) were infused iv at the onset of reperfusion for 1 h.Blood samples were taken at the end of 1 h reperfusion for determination of serum AST,ALT activities and IL-8,IL-10 concentrations.The animals were sacrificed after blood sampling.Liver specimens were obtained for determination of c-fos and c-jun expression in liver cells by immuno-histochemistry and microscopic examination with scanning electron microscope.Results Liver I/R significantly increased serum AST and ALT activities and IL-8 and IL-10 concentrations and c-fos and cjun expression in liver ceils in group Ⅱ as compared with group Ⅰ.The serum AST and ALT activities,IL-8 concentration and the c-fos and c-jun expression in liver cells were significantly lower.and the serum IL-10 concentration was significantly higher in groups Ⅲ- Ⅴ than in group Ⅱ,but there were no significant differences among the groups Ⅲ - Ⅴ.The histo-pathological changes in the liver tissue were significantly attenuated in groups Ⅲ- v as compared with group Ⅱ.Conclusion Postconditioning with remifentanil and/or propofol can attenuate liver I/R injury by inhibiting inflammatory response and apoptosis in the liver cells,but there is no significant difference in the protective effects induced by postconditioning with remifentanil or propofol alone or in combination.

Objective To investigate the effects of propofol combined with remifentanil on he-patic ischemia-reperfusion injury in cirrhotic rats.Methods Sixty male SD rats of 260 to 300 grams were randomly divided into five groups(n=12):the sham-operated group(group S);the model con-trol group (group M);propofol group (group P);remifentanil group (group R);propofol combined with remifentanil group (group PR).In group M,P,R,PR,the hepatic arteries and veins of middle and left lobes were occluded for 20 min after 1 w hepatocirrhosis by using four principal factors,and group S went through an open surgery only.In groups P,R,and PR,porpofol (at a rate 20 mg·kg-1 ·h-1 for 1 h)、remifentanil (at a rate 1 μg·kg-1·min-1 for 1 h)and porpofol (at a rate 20 mg·kg-1· h-1 )combined with remifentanil(at a rate 1 μg·kg-1·min-1 for 1 h)was infused iv at 10 min before is-chemia,respectively.In group M,normal saline was infused iv at the same rate.Blood samples were taken at the end of 4 h reperfusion to determine serum AST,ALT activity.Meanwhile liver specimens were collected to assess Bcl-2 and Bax protein expression in liver cell and measuring the apoptosis in-dex(AI)of hepatic cell.The pathological change of liver was also examined.Results Compared with group S,the activity of AST,ALT,the expression of Bcl-2 and Bax and the apoptosis index(AI)of hepatic cell of the other groups all increased significantly(P <0.05);Compared with group M,the expression of Bcl-2 of groups P,R,PR significantly increased,and the activity of AST,ALT,the ex-pression of Bax and the apoptosis index(AI)of hepatic cell significantly decreased(P <0.05 );Com-pared with groups P and R,the expression of Bcl-2 of group PR significantly increased,and the activ-ity of AST,ALT,the expression of Bax and the apoptosis index(AI)of hepatic cell significantly de-creased(P <0.05);Microscopy and scanning electron microscopy showed that,for groups P,R,PR, pathological injury of liver tissue significantly reduced compared with group M.Conclusion Propofol combined with remifentanil can reduce the hepatic ischemia-reperfusion injury in cirrhotic rat by regu-lating Bcl-2 and Bax protein expression and inhibiting apoptosis.The effect is much more enhanced when they are used in combination than individuals.

Objective To investigate the role of central and peripheral sensitization in remifentanil-induced hyperalgesia in a rat model of inflammatory pain. Methods Twenty-one male SD rats weighing 200-300 g were used in this study. Inflammatory pain was induced by intraplantar injection of 1 % carrageenan 100 fd in the left hindpaw in all animals. The animals were then randomly divided into 3 groups ( n = 7 each): control group (group C) and two remifentanil groups (group R1 , R2) . In R1 and R2 groups remifentanil was infused iv at a rate of 10 and 30 μg-kg-1·min-2 respectively starting from 5 min before till 25 min after carrageenan injection, while in group C normal saline was infused iv instead of remifentanil. Bilateral paw withdrawal threshold to mechanical stimulation with von Frey filament (PWT) was measured before (baseline) and at 1 h, 3 h and 1-7 d after carrageenan injection. Bilateral paw withdrawal latency to noxious thermal stimuli (PWL) was measured before and at 2 h, 4 h and 1-7 d after carrageenan injection. The thickness of the plantar surface of left hindpaw was measured before and at 1 h, 4 h and 1-7 d after carrageenan injection. Results Bilateral PWT was significantly lower at day 1 after carrageenan injection in R, and R2 groups than in group C. The right PWT was significantly lower at 2 d and 4-7 d after carrageenan injection in group R2 than in group R, . There was no significant difference in PWL and thickness of the plantar surface of left hindpaw among the 3 groups. Conclusion Central sensitization is involved in developing and maintaining the remifentanil-induced hyperalgesia in a rat model of inflammatory pain, while peripheral sensitization is not.

Objective:To analyze the effects of silver ion on the integration frequency of the class 1 integron in Escherichia coli ( E. coli) BL21(DE3) host. Methods:Two recombinant plasmids, pUCINT and pACINAD, were successively transformed into E. coli BL21 (DE3) to construct HS2 strains. Three experimental groups were set up using 0.3 μg/ml, 0.6 μg/ml and 0.8 μg/ml silver ion LB liquid medium, while control group used common LB liquid medium. Silver ion was supplied by silver nitrate and HS2 strains were cultured at 37℃ for 24 h. The copy number of cointegrates and the total copy number of integrons in each group were detected by real-time polymerase chain reaction (qPCR), and the ratio of them was the integration frequency. Changes in the integration frequency were analyzed by three independent phenotypic screening method and the protein expression in HS2 strains was analyzed by mass spectrometry. Results:The integration frequency in HS2 strains in the control group and three experimental groups (0.3 μg/ml, 0.6 μg/ml and 0.8 μg/ml silver ion) was 1.79×10 -5 (1.44×10 -5, 3.13×10 -5), 2.07×10 -5 (1.49×10 -5, 2.67×10 -5), 2.25×10 -6 (1.47×10 -6, 4.54×10 -6) and 1.69×10 -6 (0.22×10 -6, 3.08×10 -6), respectively. The integration frequency in the 0.6 μg/ml and 0.8 μg/ml silver ion groups was significantly lower than that in the control group ( P<0.01), but there was no significant difference between the 0.3 μg/ml silver ion group and the control group. Results of three independent phenotypic screening method were consistent with those obtained by qPCR. Mass spectrometry analysis showed that there were differences in protein expression in HS2 strains between the control group and the experimental groups. Conclusions:Silver ion at a certain concentration had an inhibitory effect on the frequency of drug resistance gene cassette captured by bacterial integron.

Objective To evaluate the effects of amiodarone on connexin43 (Cx43) expression during myocardial ischemia-reperfusion (I/R) in rats.Methods Adult male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 3 groups (n =12 each) using a random number table:shame operation group (group S),I/R group and amiodarone group (group AM).Myocardial ischemia was induced by occlusion of anterior descending branch of left coronary artery for 30 min followed by 120 min of reperfusion in I/R and AM groups.Amiodarone 5.0 mg/kg was injected intravenously at 10 min before ischemia followed by infusion at a rate of 0.15 mg· kg-1 · min 1 until the end of reperfusion.Arrhythmia was recorded during reperfusion and scored.At the end of reperfusion,blood samples were taken from the femoral artery for determination of the serum levels of cardiac troponin Ⅰ (cTnI) and creatine kinase isoenzyme-MB (CK-MB).Then the animals were sacrificed and myocardial specimens were removed for determination of the expression of Cx43 protein (by immuno-histochemistry) and mRNA (by RT-PCR) in myocardial tissues.Results Compared with group S,the arrhythmia score and serum levels of CK-MB and cTnl were significantly increased,and the expression of Cx43 protein and mRNA was downregulated in I/R and AM groups (P ＜ 0.05).Compared with group I/R,the arrhythmia score and serum levels of CK-MB and cTnI were significantly decreased,and the expression of Cx43 protein and mRNA was up-regulated in group AM (P ＜ 0.05).Myocardial Cx43 was unevenly distributed in group I/R,while evenly distributed in S and AM groups.Conclusion The mechanism by which amiodarone protects myocardium against I/R-induced arrhythmia is related to inhibition of redistribution of Cx43 and up-regulation of Cx43 expression in rats.

Objective To evaluate the role of mitochondrial permeability transition pore (mPTP) in hepatocytes in reduction of hepatic ischemia-reperfusion (I/R) injury by limb ischemic postconditioning in rats.Methods Forty-eight healthy male Sprague-Dawley rats,weighing 240-280 g,were randomly divided into 4 groups (n =12 each) using a random number table:sham operation group (group S);I/R group;limb ischemic postconditioning group (group LIPC);limb ischemic postconditioning and atractyloside group (group LIPC + APC).In I/R,LIPC and LIPC + APC groups,I/R injury was induced by 30 min occlusion of the hepatic artery and portal vein entering the left and middle lobes of the liver,followed by 120 min of reperfusion.The animals underwent 10 min of bilateral limb ischemia starting from 20 min after liver ischemia in group LIPC.In group LIPC+APC,the animals underwent 10 min of bilateral limb ischemia starting from 20 min after liver ischemia,and atractyloside 5 mg/kg was infused simultaneously via the penile vein.Blood samples were collected from inferior vena cava at the end of reperfusion to detect plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities.The rats were sacrificed,and the left lobe of the liver was removed to detect the degree of mPTP opening and to examine the ultrastructure of hepatocytes under electron microscope.Results Compared with group S,the plasma ALT and AST activities and degree of mPTP opening were significantly increased,and the damage to the ultrastructure of hepatocytes was obvious in the other three groups.Compared with group I/R,the plasma ALT and AST activities and degree of mPTP opening were significantly decreased,and the damage to the ultrastructure of hepatocytes was reduced in LIPC and LIPC + APC groups.Compared with group LIPC,the plasma ALT and AST activities and degree of mPTP opening were significantly increased in group LIPC+APC.Conclusion Limb ischemic postconditioning reduces hepatic I/R injury through inhibiting mPTP opening in hepatocytes of rats.

ObjectiveTo investigate the effect of remifentanil on hepatic ischemia-reperfusion (I/R) injury in rats with liver cirrhosis.MethodsThirty male SD rats weighing 260-300 g were randomly divided into 3 groups (n =10 each):group liver cirrhosis (group C); group liver cirrhosis + hepatic I/R (group I/R) and group remifentanil (group R).Liver cirrhosis was produced in all animals in the 3 goups.I/R injury was induced by 20 min occlusion of the hepatic artery and portal vein entering the middle and left lobes of the liver followed by 4 h reperfusion at 1 week after establishment of hepatic cirrhosis in I/R and R groups.In group R remifentanil was infused iv at 1 μg·kg-1 ·min-1 starting from 10 min before ischemia until the end of 4 h reperfusion.Venous blood samples were taken from inferior vena cava at the end of 4 h reperfusion for measurement of serum ALT and AST activities.The animals were then sacrificed and liver specimens were taken from middle lobe for determination of Bcl-2 and Bax expression (by immuno-histochemistry) and hepatocyte apoptosis (by TUNEL) and microscopic examination.Apoptosis index (percentage of apoptotic cells) was calculated.ResultsI/R significantly increased serum ALT and AST activities,Bax expression and apoptosis index and decreased Bcl-2 expression in group I/R as compared with group C.Remifentanil significantly attenuated the I/R-induced changes in serum ALT and AST activities,Bax and Bcl-2 expression and apoptosis in group R as compared with group I/R.Remifentanil also ameliorated I/R-induced liver damage.ConclusionRemifentanil can auenuate hepatic I/R injury in rats with liver cirrhosis by up-regulating Bcl-2 expression and down-regulating Bax expression and inhibiting apoptosis.

Strokes due to atrial fibrillation (AF) are common and frequently devastating.While oral anticoagulant agents are the mainstay in the prevention of embolic events,they have several limitations and not all patients can tolerate them long term.The left atrial appendage (LAA) has been identified as the source of thrombus formation in nonvalvular AF.Several LAA closure devices have been developed,they have been successful in stroke prevention in patients with nonvalvular AF and fewer periprocedural complications.This article reviews the application of percutaneous left atrial appendage closure for stroke prevention in patients with nonvalvular AF.

Objective To observe and explore clinical efficacy ofTianma-Gouteng decoction combined valsartan in the treatment of patients with renal hypertension and its effects on renal function. Methods A total of 130 patients with renal hypertension were enrolled and randomly divided into a study group (68 patients) and a control group (62 patients). Both groups were given prescription of lower sodium diet, exercising and enalaprilscheme. On this basis, the control group plus valsartan, and the study group was further added withTianma-Gouteng decoction. After 2 courses treatment, renal function, and blood pressure of both groups were compared, and clinical efficacy on blood pressure were evaluated.Results After treatment, the SBP (126.8 ± 9.1 mmHg vs. 134.1 ± 8.8 mmHg,t=4.648), DBP (82.4± 5.0 mmHgvs. 85.3 ± 5.4 mmHg, t=3.167), Scr (148.5 ± 46.3μmol/Lvs. 172.1 ± 52.0μmol/L, t=2.723), BUN (8.3 ± 2.7 mmol/Lvs. 9.7 ± 3.1 mmol/L,t=2.734) and 24hAlb (1.7 ± 0.6 gvs. 1.9 ± 0.7 g,t=2.209) in the study group were significantly lower than control group (P<0.05 orP<0.01). The total effective rate in the study group was significantly increased than that in the control group (91.2%vs. 79.0%;χ2=0.383,P=0.050).Conclusion Valsartan combined with Tianma-Gouteng decocntion can reduce blood pressure, and alleviate the kidney damage effectively.

Objective To investigate the clinical effect ofYishen-Lishi formula combined with conventional treatment for gouty nephropathy.MethodsA total of 118 patients with gout nephropathy were included and divided randomly into a conventional treatment group (n=60) and a combined treatment group (n=58) according to the random number table method. The patients in the conventional treatment group were treated with allopurinol and those in the combined treatment group were treated with allopurinol and Yishen-Lishi formula, both for 3 months. Serum uric acid, blood urea nitrogen (BUN), serum creatinine (SCr), 24 h endogenous creatinine clearance (CCr), 24 h urine protein, urineb2 microglobulin, serum triacylglycerol (TG), serum total cholesterol (TC), serum apolipoprotein A1, 24 h urine volume and urine pH were determined. The therapeutic effect was evaluated.ResultsThe urine pH (6.43 ± 0.6vs.6.21 ± 0.4;t=2.351,P=0.020), 24 h urine volume (3.3 ± 0.4vs.2.8 ± 0.6 L;t=5.308,P<0.001), 24 h CCr (1.61 ± 0.11 ml/svs. 1.33 ± 0.10 ml/s;t=14.477,P<0.001) and serum apolipoprotein A1 (1.90 ± 0.40 g/Lvs. 1.01 ± 0.33 g/L;t=13.203,P<0.01) in the combined treatment groupwere significantly higher than those in the standard treatment group. The serum uric acid (312.01 ± 33.56mmol/Lvs.350.12 ± 35.21 mol/L;t=6.015,P<0.001), BUN (6.22 ± 0.91 mmol/Lvs.11.50 ± 4.01 mmol/L;t=9.586,P<0.001), SCr (87.32 ± 13.90mmol/Lvs.122.54 ± 18.37mmol/L;t=11.743,P<0.001), 24 h urine protein (0.7 ± 0.2 gvs.1.2 ± 0.5 g;t=7.087,P<0.001), urineb2 microglobulin (220.3 ± 90.3mg/Lvs.330.1 ± 90.1mg/L;t=6.611,P<0.01), serum TG (5.11 ± 0.50 mmol/Lvs.6.30 ± 0.50 mmol/L;t=12.923,P<0.001), serum TC (1.50 ± 0.50 mmol/Lvs.2.30 ± 0.52 mmol/L;t=8.689,P<0.001) in the combined treatment group were significantly higher than those in the standard treatment group. The total effective rate inthe standard treatment group was significantly higher than those in the standard treatment group (89.7%vs.70.0%;χ2=5.871,P=0.015). ConclusionYishen-Lishi formula combined with conventional treatmentmay protect renal function, and reduce the blood lipids, its therapeutic effect is superior to conventional treatment alone in patients with gouty nephropathy.